The risk factors of portal vein thrombosis in patients with liver cirrhosis.

This study was designed to identify and assess risk factors for portal vein thrombosis (PVT) in patients with cirrhosis. A total of 98 cirrhosis patients with PVT were identified and 101 cirrhosis patients without PVT were chosen as the control group in this retrospective study. Several variables were measured and the two groups PVT and non-PVT were compared statistically. PVT was identified in 98 patients (10%). Significant differences in hematocrit, international normalized ratio, albumin, bilirubin and glucose were determined between the groups (P<0.05). Out of the thrombophilic risk factors in the patients with PVT factor V Leiden was identified in 8.8%, prothrombin gene 6.6% and methylenetetrahydrofolate reductase 2.2%. There was no difference in survival time between groups (P>0.05).

A mitochondrial neurogastrointestinal encephalomyopathy with intestinal pseudo-obstruction resulted from a novel splice site mutation.

Mitochondrial neurogastrointestinal encephalopathy (MNGIE) is an autosomal recessive disorder characterized by gastrointestinal dysmotility, cachexia, ptosis, peripheral neuropathy and leukoencephalopathy. The diagnosis is often not made until 5-10 years after the onset of symptoms. MNGIE is caused by mutations in thymidine phosphorylase gene TYMP. Here, we present a 19-year-old boy with MNGIE who had a chronic intestinal pseudo-obstruction, and we describe his family history. Genetic analysis revealed a novel homozygous c.765+1G>C intronic mutation which is expected to disrupt splicing of TYMP in the patient. Family screening revealed that the brother was also affected and the mother was a carrier. MNGIE should be considered and genetic testing instigated if individuals with cachexia have neuromuscular complaints or symptoms of chronic intestinal pseudo-obstruction.

Methylprednisolone prevents bacterial translocation in thioacetamide-induced liver failure in rats.

BACKGROUND/AIMS: Steroids have been shown to prevent intestinal oxidative stress. We investigated the effects of methylprednisolone on intestinal oxidative damage and bacterial translocation in thioacetamide-induced liver failure in rats. MATERIALS AND METHODS: Group 1 (n=8) was the control group. In group 2 (n=8), the thioacetamide group, rats received 300 mg/kg intraperitoneal thioacetamide daily for 2 days. In group 3 (n=8), the thioacetamide+methylprednisolone group, treatment with methylprednisolone (30 mg/kg intraperitoneal) was commenced 48 h before the first dose of thioacetamide. In group 4 (n=8), the methylprednisolone group, the rats received only methylprednisolone (30 mg/kg intraperitoneal). RESULTS: Serious hepatic and intestinal oxidative damage and high bacterial translocation frequencies were observed in the thioacetamide group compared with those of the controls. Bacterial translocation frequency in the thioacetamide+methylprednisolone group was significantly lower than that in the thioacetamide group (p<0.05). Intestinal thiobarbituric acid-reactive substances and myeloperoxidase levels and tissue damage scores for the intestines in the thioacetamide+methylprednisolone group were lower than those in the thioacetamide group (p<0.01, p<0.01, and p<0.0001, respectively). CONCLUSION: Our findings suggest that methylprednisolone reduces bacterial translocation by preventing intestinal oxidative damage in this model of acute liver failure in rats.

The influence of vitamin D deficiency on eradication rates of Helicobacter pylori.

BACKGROUND: Helicobacter pylori eradication therapy improves the healing of various gastro-duodenal diseases such as chronic gastritis and peptic ulcer, and also reduces gastric cancer incidence. Several studies have reported on risk factors other than antibiotic resistance related to Helicobacter pylori eradication failure. OBJECTIVES: In this study, we aimed to investigate whether or not the serum levels of 25-hydroxy-vitamin D (25(OH)D) influence eradication rates of H.pylori. MATERIAL AND METHODS: 220 patients diagnosed with H.pylori gastritis using endoscopic biopsy had their 25-OH vitamin D levels measured via the electrochemiluminescence method before beginning eradication therapy of H.pylori. Gastric biopsies obtained at endoscopy were examined for H.pylori strains and histopathologic findings. All patients were treated with bismuth-containing quadruple therapy for 14 days. H.pylori eradication was determined via the 14C-urea breath test performed 4 weeks after the end of therapy. Based on the 25-OH vitamin D levels, the patients were divided into 2 groups: group 1 (deficient) had a vitamin D level of <10 ng/mL, while group 2 (sufficient) had a vitamin D level of ≥10 ng/ mL. RESULTS: Eradication was successful in 170 (77.2%) patients and failed in 50 (22.7%) patients. The prevalence of 25(OH)D deficiency was 30.5%. Mean 25(OH)D levels were significantly lower in the eradication failure group compared to the successful treatment group (9.13 ±4.7 vs 19.03 ±8.13; p = 0.001). There were significantly more patients with deficient 25(OH)D levels in the failed treatment group compared to the successful treatment group (p = 0.001). CONCLUSIONS: Our findings suggest that 25-OH vitamin D deficiency may be considered a risk factor related to eradication failure of H.pylori, which may lead to a need for supplementation of vitamin D before eradication of H.pylori.

Association of eNOS Gene Polymorphisms G894T and T-786C with Risk of Hepatorenal Syndrome.

Background. There are no studies investigating the relationship between endothelial nitric oxide synthase (eNOS) gene polymorphisms and hepatorenal syndrome (HRS). Aim. The purpose of this study is to elucidate whether eNOS gene polymorphisms (G894T and T-786C) play a role in the development of type-2 HRS. Methods. This study was carried out in a group of 92 patients with cirrhosis (44 patients with type-2 HRS and 48 without HRS) and 50 healthy controls. Polymorphisms were determined by polymerase chain reaction (PCR) and melting curve analysis. Results. We did not find any significant difference in allele and genotype distributions of the eNOS -T-786C polymorphism among the groups (p = 0.440). However, the frequency of GT (40.9%) and TT (13.6%) genotypes and mutant allele T (34.1%) for the eNOS G894T polymorphism were significantly higher (p < 0.001 and p < 0.001, resp.) in the HRS group than in both the stable cirrhosis (14.6%, 4.2%, and 11.5%, resp.) and the control (22.0%, 2.0%, and 13.0%, resp.) groups. Conclusion. The occurrence of mutant genotypes (GT/TT) and mutant allele T in eNOS -G894T polymorphisms should be considered as a potential risk factor in cirrhotic patients with HRS.

Lighter Ingestion as an Uncommon Cause of Severe Vomiting in a Schizophrenia Patient.

Background. Foreign bodies in the gastrointestinal tract are important morbid and mortal clinical conditions. Particularly, emergency treatment is required for cutting and drilling bodies. The majority of ingested foreign bodies (80-90%) leave gastrointestinal tract without creating problems. In 10-20% of cases, intervention is absolutely required. Less than 1% of cases need surgery. In this paper, we present a schizophrenia patient who swallowed multiple lighters. Case. A 21-year-old male schizophrenic patient who uses psychotic drugs presented to the emergency department with the complaints of abdominal pain, severe vomiting, and inability to swallow for a week. His physical examination revealed epigastric tenderness. A plain radiograph of the abdomen revealed multiple tiny metallic densities. Gastroscopy was performed. The lighters were not allowing the passage, and some of them had penetrated the gastric mucosa, and bezoars were observed. One lighter was extracted with the help of the polypectomy snare. Other lighters as a bezoar were removed by surgery. Conclusion. Excessive vomiting of swallowed foreign bodies in the etiology of psychotic patients should be kept in mind. Endoscopic therapy can be performed in the early stages in these patients, but in the late stage surgery is inevitable.

Effects of rifaximin on bacterial translocation in thioacetamide-induced liver injury in rats.

Intestinal bacterial overgrowth (IBO) and increased mucosal permeability are suggested to increase bacterial translocation (BT) in liver injury. Rifaximin (RIF) is a minimally absorbed oral antimicrobial agent that restores gut microflora imbalance. The aim of the present study was to investigate the effects of RIF on BT frequency in thioacetamide (TAA)-induced liver injury. Group 1 was the control. In group 2 (TAA), rats received TAA daily for 3 days. In group 3 (TAA + RIF), RIF was commenced on the same day as the first dose of TAA. In group 4 (RIF), rats received only RIF. Ileal aspirate Escherichia coli counts were significantly lower in the TAA + RIF group than in TAA group. There was no difference in BT frequency between the TAA and TAA + RIF groups. Our results suggest that factors such as intestinal barrier dysfunction and impaired host immune shield, apart from IBO, play an important role in BT in this model.

Alterations in the pulmonary function tests of inflammatory bowel diseases.

BACKGROUND/AIMS: We aimed to determine the changes in the pulmonary function tests of the patients with inflammatory bowel diseases. METHODS: Forty inflammatory bowel dieases patients; 30 ulcerative colitis and 10 Crohn's disease, and ageand sex-matched control group, consisting of 30 healthy persons, were included in the study. Disease activity in patients with ulcerative colitis was assessed by Truelove and Witts Criteria and in Crohn's disease patients by Chron's Disease Activity Index. RESULTS: Pulmonary function tests were found abnormal at least in one parameter in 17/30 ulcerative colitis patients (56%) and in 5/10 Crohn's disease patients (50%) in the activation period and in 5/30 ulcerative colitis patients (17%) and in 2/10 Crohn's disease patients (20%) in the remission period of the diseases of the same patients. Forced vital capacity, first second, residual volume/total lung capacity, diffusing capacity of the lung for carbon monoxide and diffusing capacity of the lung for carbon monoxide per liter alveolar volume values were found significantly impaired in the activation period in comparison with the values of the same patients in the remission period (p<0.01). It was found that pulmonary function test values in patients with inflammatory bowel dieases were not affected by either the type of disease or treatment with 5-aminosalicylic acid. However, they were affected notably by the disease activity. CONCLUSION: Pulmonary function test abnormalities were found frequently in patients with inflammatory bowel dieases without presence of any respiratory symptoms and lung radiograph findings. The severity and frequency of these pulmonary function test abnormalities which were detected even in the remission periods increase with the activation of the disease. Therefore, pulmonary function test may be used as a non-invasive diagnostic procedure in determining the activation of inflammatory bowel dieases and might aid to the early diagnosis of the latent respiratory.

Prevalence of celiac disease in parents of preterm or low birthweight newborns.

AIM: Celiac disease (CD) may present with atypical symptoms, including poor pregnancy outcomes, such as preterm and low birthweight (LBW) deliveries, thus we aimed to investigate the frequency of CD in mothers and fathers of preterm or LBW newborns. MATERIALS AND METHODS: In this study, 316 parents of 164 preterm or LBW newborns and 246 parents of 123 healthy newborns were included. CD was screened using tissue transglutaminase immunoglobulin A. Endoscopic duodenal biopsy was provided in the seropositive cases. RESULTS: Positive tissue transglutaminase immunoglobulin A was found in six (1.1%; 1/94) individuals (three mothers and three fathers); five were from the study group (1.6%; 1/63) and one was from the control group (0.4%; 1/246). CD prevalence in mothers, fathers and parents of preterm newborns was 1/57 (1.8%), 1/57 (1.8%) and 1/29 (3.5%), respectively. In the LBW group, seropositivity in fathers was 1/50 (2%) with no seropositive mothers. Biopsy-proven CD was found in 1/159 mothers (0.6%) and 1/79 fathers (1.3%). Mean birthweights of the newborns of seropositive mothers and fathers were 214 g (P < 0.05) and 320 g lower than those of seronegative ones, respectively. However, in logistic regression analysis it was found that seropositivity of mothers or fathers did not affect gestational age or birthweight of the newborns. CONCLUSION: Because the prevalence of CD in parents of preterm or LBW newborns is not statistically higher than the healthy population, routine CD screening in that group cannot be recommended at the time being. For more definite conclusions further studies are needed.

An antibody of TNF-alpha did not prevent thioacetamide-induced hepatotoxicity in rats.

Tumor necrosis factor (TNF)-α antibodies have been shown to reduce liver damage in different models. We investigated the effects of infliximab (a TNF-α antibody) on liver damage in thioacetamide (TAA)-induced hepatotoxicity in rats. Group 1 (n = 8) was the control group. In group 2 (n = 8), the TAA group, the rats received 300 mg/kg intraperitoneal (ip) TAA daily for 2 days. In group 3 (n = 8), the TAA + Infliximab (INF) group, infliximab (5 mg/kg ip daily) was administered 48 hours before the first dose of TAA daily for 2 days and was maintained for 4 consecutive days. In group 4 (n = 8), the INF group, the rats received only ip infliximab (5 mg/kg) daily. Livers were excised for histopathological and biochemical tests (thiobarbituric-acid-reactive substances [TBARS], and myeloperoxidase [MPO]). Serum ammonia, aspartate transaminase (AST), alanine transaminase (ALT), TNF-α, liver TBARS and MPO levels, and liver necrosis and inflammation scores in the TAA group were significantly higher than in the control and INF groups (all p < 0.01). All parameters except AST were not significantly different between TAA and TAA + INF. In conclusion, our results suggest that oxidative stress plays an important role in TAA-induced hepatotoxicity, and infliximab does not improve oxidative liver damage.

Hypovolemia-related gastric tissue damage in the setting of upper gastrointestinal bleeding.

BACKGROUND/AIMS: Much is known about the gastric tissue damage that is associated with hypovolemic stress, but gastrointestinal bleeding due to gastric injury and further gastric injury due to hypovolemia have not been evaluated in previous research. The aim of this study was to assess oxidative gastric tissue damage specifically linked to hypovolemia in patients with upper gastrointestinal bleeding. METHODS: The study included 30 patients who presented with acute upper gastrointestinal bleeding and 30 controls. Each patient's history and laboratory findings were recorded, and multiple biopsies of the gastric antrum were obtained at diagnostic endoscopy on admission (day 1) and five days later. A set of antral biopsies was also collected from each control subject. Each tissue specimen was analyzed for levels of glutathione peroxidase, superoxide dismutase and catalase activity, and level of malondialdehyde. RESULTS: First day glutathione peroxidase, superoxide dismutase and catalase levels were significantly lower and malondialdehyde levels were higher than on the 5th day, and 1st day and 5th day levels were significantly different from controls (p<0.05). A moderate level of correlation was detected between catalase and hemoglobin (r:-0.59) and hematocrit (r:-0.61) and between malondialdehyde and systolic blood pressure (p:0.58), hematocrit (r:0.45) and hemoglobin (r:0.49). CONCLUSIONS: In this study, gastric tissue oxidative markers showed antral oxidative changes to be significantly correlated with patients' hemodynamics. Oxidative stress may not be a clinical condition but it obviously shows gastric tissue damage and may explain many of the patients' additional diagnosis of gastric erosions. Interestingly, the oxidative change does not completely recover even on the 5th day.

The relationship between severity of liver cirrhosis and pulmonary function tests.

Pulmonary complications, mainly hepatopulmonary syndrome (HPS), are frequently observed in liver cirrhosis. In this study, the aim was to investigate the frequency of hypoxemia and impairment of pulmonary function tests (PFT) in patients with liver cirrhosis and to examine the relationships of these impairments with liver failure. A total of 39 patients with cirrhosis, 24 males and 15 females, were included in our study. The mean age of the patients was 47.5 +/- 17.2 years. Arterial blood gases, PFT, and carbon monoxide diffusion tests (DLCO) were performed in all patients. Out of 39 cirrhotic patients, 21 (53.8%) had ascites, whereas 18 (46.2%) did not. Seven patients were in the Child-Pugh A group, 21 in the Child-Pugh B group, and 11 patients were in the Child-Pugh C group. Hypoxia was found in 33.3% of the patients. Although the PaO2 and SaO2 values of patients with ascites were lower compared to those without ascites (P < 0.05), no statistically significant difference was determined in the comparison of hypoxia between the groups (P > 0.05). Among the PFT parameters, FEV1/FVC and FEF25-75% values were found to be lower in patients with ascites than those without (P < 0.05). No differences were established between these two groups of patients in terms of DLCO (P > 0.05). While no differences were found in comparison of the DLCO values in between the groups (P > 0.05), there was a statistically significant difference in the ratio of DLCO to the alveolar ventilation (DLCO/VA) in between the groups (P < 0.05). On the other hand, a negative correlation was found between the DLCO/VA and Child points when the relationship between the Child-Pugh score and PFT parameters were investigated (r = -0.371, P < 0.05). Consequently, a relationship was established between the severity of liver failure and diffusion tests showing pulmonary complications invasively. We believe diffusions tests should be performed in addition to the PFT in order to determine pulmonary involvements particularly in patients who are candidates for liver transplantation.

Gastric tissue oxidative changes in portal hypertension and cirrhosis.

Gastric mucosal lesions are very common in portal hypertension and cirrhosis. The aim of this study was to assess for oxidative gastric tissue damage in cirrhosis and evaluate relations with portal hypertension and cirrhosis parameters. The study included 30 patients with cirrhosis and 30 controls. Each patient's history, physical examination, and laboratory findings were recorded, and multiple biopsies of the gastric antrum were obtained at endoscopy. A set of antral biopsies was also collected from each control subject. Each tissue specimen was analyzed for levels of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT) activity and level of malondialdehyde (MDA). Patients' gastric GPX, SOD, and CAT levels were significantly lower, and MDA levels were higher, than in the control group. The GPX activity level in the specimens was moderately negatively correlated with portal vein diameter (P<0.05, r=-0.45) and spleen length (P<0.05, r=-0.45). In this study gastric tissue oxidative markers showed that antral oxidative factors worsen in cirrhosis. Oxidative stress may not be a clinical condition but it obviously shows gastric tissue damage and may explain many patients' gastric lesions and hemorrhage.

Two findings of portal hypertension: evaluation of correlation between serum-ascites albumin gradient and esophageal varices in non-alcoholic cirrhosis.

BACKGROUND/AIMS: Esophageal varices and serum-ascites albumin gradient (SAAG) are two major findings of portal hypertension. Recently, correlation between these two findings in patients with cirrhosis due to alcohol has been attracted attention. We aimed at evaluating whether a correlation exists between these parameters in the patients with non-alcoholic cirrhosis. METHODS: Albumin levels in the serum and ascites and esophageal varices were studied and the correlation between these parameters was assessed in 45 patients with non-alcoholic cirrhosis detected between January 2002 and June 2003. RESULTS: Thirty-two of the patients were male and 13 female. The average age of the patients was 56.3+/-12.5 years (range 22-85 years). The causative agents were found to be hepatitis B virus in 35 patients and hepatitis C virus in six patients; no etiology could be determined in the remaining four patients. Serum level of albumin was determined as 2.53+/-0.53 g/dl, ascites level of albumin as 0.42+/-0.31 g/dl and SAAG as 2.1+/-0.51. Endoscopic esophageal examination revealed first-degree esophageal varices in 15 patients, second-degree esophageal varices in 18 patients and third-degree esophageal varices in eight patients; no esophageal varices could be found in four patients. There was no correlation between the degree of the esophageal varices and serum levels of albumin (p=0.7) and SAAG (p=0.2); but a weak correlation was found between the degree of the esophageal varices and ascites levels of albumin (p=0.03, r=0.30). Furthermore, the patients were classified by their SAAG values, and their varices were then assessed. Two of four patients with SAAG values between 1.1 and 1.49 had esophageal varices, as did 13 of 15 patients with SAAG values between 1.5 and 1.99, and all of the patients with SAAG values greater than 2.0. CONCLUSION: All SAAG values were greater than 1.1 in our non-alcoholic cirrhosis cases. The correlation that has been found to exist between SAAG and esophageal varices could not be found in our patients with non-alcoholic cirrhosis. It is remarkable that most of the patients with non-alcoholic cirrhosis presenting with ascites and all of the patients with an SAAG value greater than 2.0 had esophageal varices.

Quantitative Doppler evaluation of the splenoportal venous system in various stages of cirrhosis: differences between right and left portal veins.

PURPOSE: The purpose of our study was to evaluate the relationship between the splenoportal hemodynamics in patients with cirrhosis and the stage of the disease. METHODS: Patients with cirrhosis were grouped according to modified Child-Pugh scoring into stages A, B, and C of cirrhosis. A control group of healthy volunteers was included. After gastroenterologic clinical and laboratory examinations, all participants underwent a splenoportal Doppler sonographic evaluation in which the vessels' diameter, area, and blood flow velocity were measured and blood flow rate and the congestion index in the splenoportal venous system were calculated. RESULTS: Seventy-five patients with cirrhosis (25 women and 50 men) were enrolled; the control group consisted of 30 healthy volunteers (15 women and 15 men) with no liver disease. The mean age (+/- standard deviation) of the patients was 54.4 +/- 14.8 years (range, 13-80 years) and of the control subjects was 47.3 +/- 14.5 years (range, 18-72 years). No significant differences in vessel diameter, blood flow velocity, and blood flow rate were found in the main and left portal veins between the study group and the control group. In the right portal vein, we found decreases in the vessel diameter, blood flow velocity, and blood flow rate, and in the splenic vein, we found increases in vessel diameter and blood flow rate. The congestion index was increased in the main portal and splenic veins but was unchanged in the left portal vein. CONCLUSIONS: Although our data indicate that there is no difference in Doppler sonographic parameters of the main portal vein according to Child-Pugh scores, the hemodynamic differences between the left and right branches of the portal vein may be clinically useful in patients with cirrhosis.